Evidence map›Paper›PMID 17091259›Full record

ReviewEuropean journal of pediatrics2007

Familial recurrence of congenital heart disease: an overview and review of the literature.

Giulio Calcagni, M Cristina Digilio, Anna Sarkozy, Bruno Dallapiccola, Bruno Marino

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of pediatrics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Consanguinity and the risk of congenital heart disease.American journal of medical genetics. Part A · 2012
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Exome Sequencing and Congenital Heart Disease in Sub-Saharan Africa.Circulation. Genomic and precision medicine · 2021
    Article
  10. Genetic Basis of Human Congenital Heart Disease.Cold Spring Harbor perspectives in biology · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. Some Isolated Cardiac Malformations Can Be Related to Laterality Defects.Journal of cardiovascular development and disease · 2018
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Giulio CalcagniPediatric Cardiology, Department of Pediatrics, University La Sapienza, Rome, Italy.
M Cristina Digilio
Anna Sarkozy
Bruno Dallapiccola
Bruno Marino
Sapienza University of Rome · ITBambino Gesù Children's Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Familial recurrence is one of the classic patterns for the clinical presentation of congenital heart disease (CHD). In recent years, many groups studied empiric recurrence risk in these heart defects, and the aim of this review was to analyse the patterns of inheritance detected in different types of CHD, including atrioventricular canal defect, tetralogy of Fallot, transposition of the great arteries, left-sided obstructions and atrial septal defect. These studies may influence clinical practise guidelines through accurate genetic counselling, but also, they may have important implications in the knowledge of genetic and pathogenetic mechanisms of CHD.

Indexed as

FamilyGenetic Predisposition to DiseaseHeart Defects, CongenitalHumansRecurrence

Identifiers

PMID17091259
OpenAlexW2073685728

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.